Key result
Obesity-associated insulin resistance is driven by latent inflammation, adipocyte hypertrophy, and reduced regenerative potential of fat progenitor cells.
Why the study?
Obesity is a major risk factor for type 2 diabetes and metabolic syndrome, involving disturbances in normal fat tissue physiology.
This review summarizes the mechanisms linking obesity to insulin resistance, emphasizing the roles of latent inflammation and impaired adipocyte renewal.
Answers are grounded in this paper and cite their sources.
Latent inflammation may inform mechanistic studies of insulin resistance; leaves open targeted trials before clinical application.
Obesity is a major risk factor for type 2 diabetes and metabolic syndrome and an essential medical and social problem. In the first part of the review, we briefly highlight the biochemical basis of metabolic disbalance in obesity and evolution of our views on the mechanisms of insulin resistance development in insulin-sensitive tissues. Because obesity relates to the disturbance in the normal physiology of fat tissue, the second part of the review focuses on latent inflammation that develops in obesity and is supported by immune cells. Finally, the problem of adipocyte hypertrophy, reduced regenerative potential of fat progenitor cells, and impaired renewal of fat depots is discussed in the context of type 2 diabetes pathogenesis.
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Vorotnikov et al. (2019) conducted a review in Obesity and type 2 diabetes. Obesity was evaluated. Obesity-associated insulin resistance is driven by latent inflammation, adipocyte hypertrophy, and reduced regenerative potential of fat progenitor cells.
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